ReviewInternational journal of molecular sciences2023
Therapeutic Potential of Tumor Metabolic Reprogramming in Triple-Negative Breast Cancer.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 42 citations in OpenAlex.
- Review
- Special Issue "Breast Cancer: From Pathophysiology to Novel Therapies".International journal of molecular sciences · 2026Article
- Anticancer Effect of Pacificusoside D from the StarfishMarine drugs · 2026Article
- Article
- Tumor-Associated Neutrophils and Desmoplastic Reaction in the Breast Cancer Tumor Microenvironment: A Comprehensive Review.Cancers · 2026Review
- Advances in plasma metabolomics detection technology and its clinical applications in lung cancer and other malignancies.Holistic integrative oncology. · 2026Review
- Establishing and validating a new metabolic marker-driven prognosis signature for cutaneous melanoma.Scientific reports · 2025Article
- Fucosylated N-Glycan Landscape of Triple-Negative Breast Cancer.Molecular cancer research : MCR · 2025Article
- Dual-Target Therapeutic Strategies in Triple-Negative Breast Cancer: Mechanistic Insights and Clinical Potential.Cancers · 2025Review
- Neutrophils and cancer immunotherapy: Potential mechanisms and challenges in breast cancer - a narrative review.Medicine · 2025Review
- Metabolomic Effects and Their Relationship with Intracellular/Extracellular Concentrations of CasiopeinasInternational journal of molecular sciences · 2025Article
- The balance between N1 and N2 neutrophils implications for breast cancer immunotherapy: a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Nidogen-1 suppresses cell proliferation, migration, and glycolysis via integrin β1-mediated HIF-1α downregulation in triple-negative breast cancer.Scientific reports · 2025Article
- Article
- Ultrasound genomics related mitochondrial gene signature for prognosis and neoadjuvant chemotherapy resistance in triple negative breast cancer.Oncology research · 2025Article
- Caveolin-1 knockout mitigates breast cancer metastasis to the lungs via integrin α3 dysregulation in 4T1-induced syngeneic breast cancer model.Cancer gene therapy · 2024Article
- Interactions between hedgehog signaling pathway and the complex tumor microenvironment in breast cancer: current knowledge and therapeutic promises.Cell communication and signaling : CCS · 2024Review
- Triple Negative Breast Cancer: Molecular Subtype-Specific Immune Landscapes with Therapeutic Implications.Cancers · 2024Review
- CD24 negativity reprograms mitochondrial metabolism to PPARα and NF-κB-driven fatty acid β-oxidation in triple-negative breast cancer.Cancer letters · 2024Article
- Repurposing of Strychnine as the Potential Inhibitors of Aldo-keto Reductase Family 1 Members B1 and B10: Computational Modeling and Pharmacokinetic Analysis.The protein journal · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
Abstract
Triple-negative breast cancer (TNBC) is the most aggressive subtype of breast cancer, with clinical features of high metastatic potential, susceptibility to relapse, and poor prognosis. TNBC lacks the expression of the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). It is characterized by genomic and transcriptional heterogeneity and a tumor microenvironment (TME) with the presence of high levels of stromal tumor-infiltrating lymphocytes (TILs), immunogenicity, and an important immunosuppressive landscape. Recent evidence suggests that metabolic changes in the TME play a key role in molding tumor development by impacting the stromal and immune cell fractions, TME composition, and activation. Hence, a complex inter-talk between metabolic and TME signaling in TNBC exists, highlighting the possibility of uncovering and investigating novel therapeutic targets. A better understanding of the interaction between the TME and tumor cells, and the underlying molecular mechanisms of cell-cell communication signaling, may uncover additional targets for better therapeutic strategies in TNBC treatment. In this review, we aim to discuss the mechanisms in tumor metabolic reprogramming, linking these changes to potential targetable molecular mechanisms to generate new, physical science-inspired clinical translational insights for the cure of TNBC.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.